Inflammation refers to a localized, protective response to trauma or microbial invasion to remove the injurious stimuli and initiate the healing process for the tissue. Deficiencies of inflammation render a patient vulnerable to pathogen infections. Excessive inflammation caused by abnormal recognition of host tissues as foreign, on the other hand, may lead to various inflammatory diseases, e.g., atherosclerosis and rheumatoid arthritis (RA).
Atherosclerosis is a chronic inflammatory disease in which fatty materials aggregate along the walls of arteries to form atherosclerotic plaques. It is suggested that foam cell macrophages play an important role in the progress of this disease. They secret various types of cytokines and chemokines, which direct and amplify local immune responses. Several chemokines and cytokines have been found to be expressed at elevated levels at atherosclerotic lesions, suggesting their involvement in disease development.
RA is the most common form of inflammatory arthritis characterized by intense inflammation in synovial joints, causing infiltration of mononuclear phagocytes, lymphocyts, and neutrophils into synovial membranes. Recent studies show that cytokines and chemokines, such as tumor necrosis factor α (TNFα), interleukin-1β (IL-1β), IL-6, and IL-8, are substantially involved in disease progression
IL-20 is a newly discovered member of the IL-10 family. Other members of this family have been found to be crucial in the development of many inflammatory diseases, e.g., RA. IL-20 selectively increases levels of multipotential hematopoietic progenitors. It also induces the proliferation of keratinocytes, which in turn over-express proinflammatory genes.